Adrenal splanchnic innervation modulates adrenal cortical responses to dehydration stress in rats.

摘要

Classically, the production of glucocorticoids by the adrenal gland is thought to be controlled exclusively by adrenocorticotropic hormone (ACTH). However, there are several examples in stressed humans and animals of increased plasma glucocorticoids in the absence of increased plasma ACTH, suggesting that an additional, non-ACTH mechanism(s) may contribute to the control of glucocorticoid production. The present studies were designed to determine the role of the thoracic splanchnic nerve in controlling plasma corticosterone levels in response to chronic water deprivation in rats, a model previously reported to demonstrate dissociations between plasma corticosterone and ACTH. Briefly, rats underwent right unilateral adrenalectomy and left thoracic splanchnic nerve transection or sham transection. After recovery, rats were water deprived for 48 h or given free access to water, and then sacrificed for collection of plasma and adrenal glands. Water deprivation resulted in consistent, robust increases in plasma corticosterone that were attenuated by splanchnic nerve transection, in the absence of changes in post-dehydration plasma ACTH. Adrenal content of steroidogenic acute regulatory factor (StAR) and cyclic AMP (cAMP) were increased after dehydration; splanchnic nerve transection decreased post-dehydration adrenal cAMP, but not StAR. Splanchnic nerve transection also attenuated plasma corticosterone responses to submaximal doses of ACTH in dexamethasone-blocked, dehydrated rats, suggesting a decreased adrenal sensitivity to ACTH. Collectively, the present results demonstrate that the thoracic splanchnic nerve normally augments the adrenal corticosterone response to dehydration stress by increasing adrenal sensitivity to ACTH, and this augmentation is associated with elevations in adrenal cAMP content. These data support the hypothesis that the splanchnic innervation of the adrenal gland represents an additional physiological mechanism to control stress-induced adrenal cortical responses in vivo.